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Biomedical subjects

R Rubio

Publications and source records attributed to R Rubio.

At least 91 records · Page 5Linked to original sources
PubMed1995

Coculture of astroglial and vascular endothelial cells as apposing layers enhances the transcellular transport of hypoxanthine.

In brain, astrocytes and endothelial cells are a major site of adenosine degradation. These two cell types, found in close apposition, constitute the wall of the brain's capillaries and serve as a site of hypoxanthine production and degradation. Both cell types possess the hypoxanthine salvage pathway and can incorporate hypoxanthine into nucleotides. This suggests that the endothelial-astrocyte anatomical complex might play an important role in the brain's purine homeostasis. To test this hypothesis, cocultures of monolayers of vascular endothelial cells and astrocytes were grown over a porous membrane, in close apposition to one another, and studies on hypoxanthine transport and metabolism to uric acid were performed. The flux of hypoxanthine across the cell layers was simultaneously determined and compared with the flux of sucrose, as a probe of passive diffusion. Our results show that in endothelial, glial, and endothelial-glial cell layers the hypoxanthine flux was greater than that of sucrose, and that the flux of hypoxanthine, but not of sucrose, was inhibited by adenine or by lowering the temperature. These results suggest that hypoxanthine moves across endothelial, glial, and endothelial-glial cell layers by a transport process. Furthermore, we found that hypoxanthine transport is enhanced when glial and endothelial cells are cocultured compared with that in glial or endothelial monolayers. In addition the coculture also resulted in a depression of xanthine oxidase activity.

Adenine↗
PubMed1995

Coronary flow stimulates auricular-ventricular transmission in the isolated perfused guinea pig heart.

In the heart in situ coronary flow stimulates oxygen consumption, glycolytic flux, myocardial contractility, and the release of bioactive substances. Studies have indicated that the coronary flow-enhanced contraction is similar to a hormonelike effect because the enhanced contraction results from an elevation in intracellular free calcium. In fact, if extracellular calcium is raised sufficiently, the contraction amplitude rises and remains constant and independent of coronary flow. We hypothesized that coronary flow could also stimulate other calcium-dependent cardiac functions such as auricular-ventricular (A-V) transmission. This hypothesis was tested in isolated guinea pig hearts perfused at constant flow. Our results show that increases in coronary flow (6-25 ml/min range) decrease the A-V delay solely as a result of reduced propagation time in the A-V node and not in atrial or ventricular propagation. When coronary vascular resistance was altered by dilation (nitroglycerin, bradykinin, nitroprusside, and adenosine) or by constriction (angiotensin II), this dromotropic effect of flow remained the same despite wide changes in perfusing pressure. Also, this dromotropic effect of flow was not altered by energy-altering substrates in the perfusate or by perfusion of adenosine receptor blockers. Furthermore, the effectiveness of flow as a dromotropic stimulus varied inversely with changes in calcium entry caused either by elevation or reduction of extracellular calcium. In addition, enhanced viscosity of the perfusing medium amplifies the positive dromotropic effect of flow. These results suggest that coronary flow is a stimulus that exerts a positive dromotropic effect mediated by shear stress.

Aminophylline↗
PubMed1995

[Why the cardiologists should be interested in lipids?].

This review discuss the possible 10 top reasons why cardiologists are/should be interested in lipids. 1. Epidemiologic evidence. Blood lipid levels are risk factors for coronary heart disease and predict subsequent mortality in the patients seen by cardiologists. 2. Lipids play a major physiopathologic role in ischemic heart disease. Stenosis of the coronary arteries are produced by atherosclerotic plaques, composed of a mass of lipids covered by a fibrous cap. Plaques with increased lipid content appear more prone to rupture and cause acute coronary syndromes. 3. Lipid abnormalities are very common in patients with ischemic heart disease. At least half the patients with angiographic evidence of significant coronary artery narrowings have severe abnormalities of lipids that are easy (and cheap) to detect. 4. Reduction of cholesterol is associated with regression of atherosclerosis, as has been demonstrated by angiography in patients with coronary heart disease. 5. Reduction of cholesterol is associated with reduction of symptoms and ischemic events. 6. The most striking benefit of lipid lowering therapy is shown in patients, already with evidence of ischemic heart disease. 7. The new lipid lowering agents present a new profile of actions and may improve symptoms in the short term. 8. There is still controversy about who should be treated, when and with what drugs, and this questions will be solved with the evidence of large, multicenter, well designed trials that are now in progress. Cardiologists must contribute to this studies, know and discuss the results. 9. If a patient is not given by his cardiologist any drug to reduce the cholesterol it is quite improbable that other doctor would make such recommendation. 10. Even if the cardiologist is not interested in lipids their patients are, and seek and deserve advice.

Adult↗
PubMed1995

[Cardiovascular pharmacology (XIII). The efficacy of different thrombolytic drugs in the treatment of acute myocardial infarct].

In patients with acute myocardial infarction (AMI) thrombolysis reduces the infarct area, preserves ventricular function and improves survival. This effect is more significant in men with age between 65 and 75 years, anterior ST segment elevation or branch block, during the first 6 hours of evolution. In this review the comparative studies with placebo and between different fibrinolytic agents, in different doses or in combination are reviewed, and the drug selection, the actual impact or fibrinolysis and future directions of thrombolysis in patients with AMI are discussed. Reperfusion is highest with the use of double bolus tPA of front-loaded rapid tPA infusion. Reocclusion is more frequent after tPA and minimal after urokinase or the combination of tPA and urokinase. In the GISSI-2 and ISIS-3 studies, the mortality of patients treated with streptokinase, tPA or APSAC was similar. However, in the GUSTO study, with front loaded, rapid infusion of tPA, mortality was lower than with streptokinase, although this effect was only statistically significant in patients with anterior infarction or age < 75 years. Bleeding is more common with tPA, and allergic reactions are more frequent after streptokinase and APSAC than after tPA or urokinase. Symptomatic hypotension and bradycardia are also more frequent after streptokinase or APSAC, specially in patients with right ventricular infarction. Streptokinase and APSAC generate antibodies that may neutralize the effect of a second administration even years after the first dose. On the basis of the current clinical evidence it is not possible to recommend the use of a single fibrinolytic and, due to its lowest cost, streptokinase could be considered the first choice. However, in patients with previous thrombolysis, as well as in those with right ventricular infarction, the drug of choice should be tPA or urokinase; in young patients with anterior infarction tPA is more effective and in patients with difficult controls (mobile CCU, emergency wards, etc.) APSAC or urokinase may be considered the agent of choice because their easier administration. In spite of clear evidence of the efficacy of the thrombolytic therapy, it is only used in 20%-30% of the patients with AMI, and probably there is a selection of low risk patients. For these reasons, the impact of thrombolysis in the whole population of AMI is probably lower than it could be. Future directions for the use of thrombolytic agents include a better selection of the candidates and the drug to be used as well as the early administration of thrombolytics, even before the admission to the CCU.

Aged↗
PubMed1994

Hodgkin's disease associated with human immunodeficiency virus infection. A clinical study of 46 cases. Cooperative Study Group of Malignancies Associated with HIV Infection of Madrid.

BACKGROUND: Hogdkin's disease is not an acquired immunodeficiency syndrome (AIDS)-defining illness. However, Hodgkin's disease associated with human immunodeficiency virus (HIV) infection has a different natural history and therapeutic outcome than in the general population of Hodgkin's disease patients. METHODS: The authors studied the epidemiologic and clinicopathologic features and therapeutic outcomes of 46 patients with Hodgkin's disease associated with HIV infection collected from a cooperative study of nine hospitals in Madrid, Spain. RESULTS: Forty-three (93.5%) of the subjects were men and three (6.5%) were women, with a mean age of 26.9 years. Thirty-nine (84.8%) were intravenous drug users and four (8.7%) were homosexuals. In 43 patients (93.5%), Hodgkin's disease was the first manifestation of HIV infection. In 16 patients (34.8%), AIDS developed after the diagnosis of Hodgkin's disease. Histologic subtypes were mixed cellularity (41.3%), lymphoid depletion (21.7%), nodular sclerosis (21.7%), and lymphocytic predominance (4.3%). At diagnosis, 89.1% had advanced stages (III,IV), 82.6% had B symptoms, and 41.3% had bone marrow involvement. Of 27 evaluable patients treated with chemotherapy, 44.4% had a complete response (16.7% relapsed) and 37% had a partial response. Median survival was 15 months (range, 1-44 months). Projected 3-year survival rate was 19%, and projected event-free survival rate was 22% at 30 months. Adverse prognostic factors for survival in univariate analysis were B symptoms, no response to chemotherapy, hemoglobin levels less than 11 g/dl, leukocyte count less than 4500/mm3, total lymphocyte count less than 1000/mm3, CD4 lymphocyte count less than 200/mm3, and alkaline phosphatase level greater than 300 IU/l. CONCLUSIONS: Hodgkin's disease associated with HIV infection is more frequent among intravenous drug addicts, and the clinical course is different in these patients from that in the general population of Hodgkin's disease patients, showing high frequency of advanced stages, unfavorable histologic subtypes, poor therapeutic response, and short survival time.

AIDS-Related Opportunistic Infections↗
PubMed1994

Differential distribution of purine metabolizing enzymes between glia and neurons.

Previous studies showed that in cultured chick ciliary ganglion neurons and CNS glia, adenosine can be synthesized by hydrolysis of 5'-AMP and that the accumulation of the adenosine degradative products inosine and hypoxanthine was significantly greater in glial than in neuronal cultures. Furthermore, previous immunochemical and histochemical studies in brain showed that adenosine deaminase and nucleoside phosphorylase are localized in endothelial and glial cells but are absent in neurons; however, adenosine deaminase may be found in a few neurons in discrete brain regions. These results suggested that adenosine degradative pathways may be more active in glia. Thus, we have determined if there is a differential distribution of adenosine deaminase, nucleoside phosphorylase, and xanthine oxidase enzyme fluxes in glia, comparing primary cultures of central and ciliary ganglion neurons and glial cells from chick embryos. Hypoxanthine-guanine phosphoribosyltransferase and production of adenosine by S-adenosylhomocysteine hydrolase activity were also examined. Our results show that there is a distinct profile of purine metabolizing enzymes for glia and neurons in culture. Both cell types have an S-adenosylhomocysteine hydrolase, but it was more active in neurons than in glia. In contrast, in glia the enzymatic activities of xanthine oxidase (443 +/- 61 pmol/min/10(7) cells), nucleoside phosphorylase (187 +/- 8 pmol/min/10(7) cells), and adenosine deaminase (233 +/- 32 pmol/min/10(7) cells) were more active at least 100, 20, and five times, respectively, than in ciliary ganglion neurons and 100, 100, and nine times, respectively, than in central neurons.

Adenosine↗
PubMed1994

Possible role of nitric oxide in catecholamine secretion by chromaffin cells in the presence and absence of cultured endothelial cells.

We studied the effect of cultured endothelial cells on the secretion of catecholamines by cultured bovine chromaffin cells. Chromaffin cell catecholamine secretion was stimulated by either boluses of potassium (K+) or the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP). Endothelial cells inhibited the catecholamine release and stimulatory effects of K+ and DMPP. This inhibition increased with time, and in 25 min the initial stimulated secretory response (100%) to 30 mM K+ or 25 microM DMPP dropped to 45 +/- 3% and 53.5 +/- 2.3%, respectively. This endothelial cells-induced inhibition was blocked by the nitric oxide synthase inhibitors N-nitro-L-arginine methyl ester (L-NAME) and N-monoethyl-L-arginine (L-NMMA), and by the guanylate cyclase inhibitor methylene blue, indicating that the L-arginine/nitric oxide/cyclic GMP pathway is involved in this endothelial cell-chromaffin cell interaction. In the absence of endothelial cells, incubation of chromaffin cells with L-NAME, L-NMMA, or methylene blue also augmented the secretagogue-induced catecholamine secretion, indicating that nitric oxide from chromaffin cells could be implicated in an autoinhibitory process of catecholamine release. These results provide indirect evidence for the presence of nitric oxide synthase in bovine adrenomedullary chromaffin cells. Our results show that there is an autoinhibitory mechanism of catecholamine release in chromaffin cells and that an additional level of inhibition is observed when cultured vascular endothelial cells are present. These two inhibitory processes may have different origins, but they appear to converge into a common pathway, the L-arginine/nitric oxide synthase/guanylate cyclase pathway.

Adrenal Medulla↗
PubMed1994

[Liver cirrhosis and pregnancy].

A clinical case of a woman 25 year old with Laennec's cirrhosis at 18th, week of gestation was admitted in our hospital. In the 30th week a cesarean section was performed, resulting a healthy infant. The infrequency relationship between pregnancy and cirrhosis is discussed an a review of the literature is presented.

Adult↗
PubMed1994

[Radiofrequency fulguration of accessory pathways].

Between August 1991 and August 1993, 75 patients (42 male) with Wolff Parkinson White syndrome (43 concealed) were subjected to radiofrequency ablation of accessory pathways at our institution. 55 had left, 8 postero septal, 2 anteroseptal and 10 right accessory pathways. A retrograde aortic technique with placement of the ablation catheter in close proximity to the mitral annulus was used for most of the patients with left accessory pathways and for some with posteroseptal pathways. The right, anteroseptal and some posteroseptal pathways were ablated using a right heart approach placing the ablation catheter in the tricuspid annulus. Ablation was successful in 61 patients (81%). One subject developed a fatal cardiac tamponade after a transeptal catheterization and was unrelated to the ablation per se. It is concluded that radiofrequency ablation of accessory pathways is a curative procedure for a great majority of patients with Wolf Parkinson White syndrome.

Adolescent↗
PubMed1993

[Thromboangiitis obliterans (Buerger's disease). Study of 41 cases].

BACKGROUND: The aim of this study was to know the prevalence, clinical and immunological characteristics and evolution of thromboangiitis obliterans. METHODS: Between 1982-1990 41 cases of thromboangiitis obliterans were diagnosed from among 373,899 patients registered (11/100,000) according to the clinical and arteriographic criteria. Of these 41 cases 40 were males with mean age 36 +/- 7 years (mean +/- SD) with only two cases being over 45 years of age. In 40 cases was followed for 44 +/- 29 months (mean +/- SD). RESULTS: All the patients had ischemia of the lower limbs, 34% of the upper limbs, 39% superficial thrombophlebitis, 53% Raynaud's phenomenon, 5% mesenteric ischemia, and 7% myocardial infarction. In 30 symptomatic patients anticardiolipin antibodies were determined and one patient was positive for IgG antibodies. In the 23 patients in whom HLA and anticollagen antibody studies were performed a significant increase was found in HLA-B35, HLA-B40 and type VI denaturalized anticollagen antibodies compared to controls. In general the evolution was progressive when the patients continued smoking and favorable when tobacco was given up except in 2 cases who stopped smoking and in whom the disease progressed and death occurred. The total number of patients who died during follow up was 3 (7%), 2 due to mesenteric ischemia and the third during i.v. infusion of PGE1. CONCLUSIONS: The results demonstrate that thromboangiitis obliterans is a rare disease in Spain. The involvement of visceral arteries is not very infrequent with worse prognosis when the mesenteric arteries are involved. There is a significant increase of determined HLA antigens and anticollagen antibodies in the patients with thromboangiitis obliterans.

Adult↗
PubMed1993

Implications of the coronary vascular endothelium as mediator of the vasodilatory and dromotropic actions of adenosine.

Recent studies have shown that the vasodilatory response of adenosine is partially endothelium dependent. Therefore, to further characterize the physiologic role of the vascular endothelium as mediator of adenosine's cardiovascular effects, we have examined in isolated perfused guinea-pig hearts the dromotropic and vascular effects of adenosine in the presence of the adenosine antagonist, XAC, covalently conjugated to latex microspheres of 0.07 microns diameter. Our results demonstrate that intravascular infusion of the microsphere XAC conjugates abolishes the vasodilatory and negative dromotropic effects of infused adenosine, and inhibits the dromotropic effects of hypoxia. As these particles because of their size remain intravascularly confined, we conclude that the dromotropic and vasodilatory effects of exogenous adenosine, and the dromotropic effects of hypoxia (endogenous adenosine), arise from the intravascular adenosine compartment acting by way of the vascular endothelium. In addition, while neither the temporal course of vasodilation nor the steady state of vasodilation caused by hypoxia were influenced by unconjugated XAC, our results do show that the microsphere XAC conjugate increases the time necessary for maximum vasodilation to occur during hypoxia.

Adenosine↗
PubMed1993

[Block of the slow pathway of the double atrioventricular node: a new technique for treatment of atrioventricular node reentry tachycardia].

The aim of this work is to summarize the first experience in Chile modifying the slow pathway in patients with tachycardias due to atrio-ventricular node reentry. Until now, the only available treatment was the use of antiarrhythmic drugs. The radiofrequency fulguration or cauterization of part of the atrioventricular node has been reported as a treatment for these arrhythmias. The initial technique fulgurated the rapid pathway with a significant risk of atrioventricular block. The modification of the slow pathway has been recently described. We report two patients, 9 and 45 years old, with a history of recurrent tachycardias, refractory to pharmacological treatment. An electrophysiological study demonstrated that the mechanism of their arrhythmias was a nodal reentry. In the same session one of the mapping catheters was changed by a fulguration one and radiofrequency was applied, using a variation of the technique described by Jackman. In both, the slow pathway was modified or blocked with definitive interruption of the nodal reentry circuit and preservation of atrioventricular conduction.

Catheter Ablation↗
PubMed1993

[The progression of a postinfarct interventricular communication: an echocardiographic follow-up].

An 80-year-old female patient presented rupture of the interventricular septum as complication of acute anteroseptal myocardial infarction. Serial echocardiographic studies documented progressive increase in size of the apical defect over 16 hours. This observation highlights a potential hazard if surgical repair is deferred to "stabilize" hemodynamically the patient before the intervention.

Aged↗
PubMed1992

Functional role of intravascular coronary endothelial adenosine receptors.

The endothelium is relatively 'impermeable' to adenosine. In addition, infusion of adenosine deaminase and transient infusion of large size adenosine agonists (molecular weight 100 kD) which are confined to the intravascular space depress effects of endogenous adenosine and retain physiologic activity respectively. Accordingly, the concept that intravascular adenosine may exert some of its action on the capillary lumen was tested by coupling the agonists: N6-([aminoethylamino]carbonyl)methylphenyladenosine (ADAC) and N6-octylamine adenosine (NOA) to carboxylated latex microspheres (0.07 microns diameter); thus, insuring their intravascular confinement. Our results demonstrated that sustained infusion of these particles into isolated saline perfused guinea pigs hearts caused a decrease in coronary vascular resistance, ventricular contraction, spontaneous ventricular rhythm, inhibition of auricular ventricular transmission and glycolytic flux. These effects were reversible and specific since microspheres without purines had no effect and the adenosine antagonist sulphophenyltheophylline blocked these responses. Furthermore, the effects were not the result that during the passage of the sphere-agonist complex through the heart the covalent bond hydrolyzed, releasing free agonist. Our data indicate that selective activation of intravascular coronary purine receptors may cause the release of endothelial bioactive messengers that regulate the function and metabolism of vascular and cardiac cells.

Adenosine↗
PubMed1992

Heterogeneity and sampling volume dependence of epicardial adenosine concentrations.

Rapid steady-state estimates of interstitial fluid (ISF) adenosine concentrations (ADOi) in the left ventricular epicardium of anesthetized dogs were obtained by the epicardial porous disc (EPD) method described herein. Because of the high temporal and spatial resolution of this method, it was ideally suited to test the hypothesis that ADOi may vary in these domains. Variance in steady-state EPD solute concentrations was quantified statistically by the coefficient of variation (CV = standard deviation/mean), which we used as an index of heterogeneity. A significant temporal variation in steady-state EPD adenosine concentrations was observed when samples were sequentially collected from one epicardial location (CV = 42.9 +/- 3.5%). When steady-state sample pairs (n = 45) were collected simultaneously from two distinct epicardial locations, a 2.6 +/- 0.3-fold mean difference in their respective adenosine concentrations was measured. About 25% of this variation was inherent in procedural methodology, based on the variability of steady-state EPD concentrations of extracellularly-equilibrated 14C sucrose (CV = 12.7 +/- 1.2%) and the variability of steady-state concentrations of both solutes measured using in vitro preparations (mean CV = 9.7 +/- 1.2%). Thus, we contend that endogenous myocardial ISF adenosine is temporally and perhaps spatially heterogeneous. Our estimates of steady-state ADOi obtained with the EPD method ranged from 0.47 to 0.99 microM. Using modifications of the EPD technique and the epicardial chamber, we also demonstrated that the adenosine concentration in 'steady-state' epicardial samples is reduced when the volume/surface area ratio of the sample buffer is increased. We hypothesize that sampling-induced decreases in steady-state ADOi underlie these observations, because losses of ISF adenosine to high volumes of sample buffer can be greater than the myocardial cells are capable of replacing. However, with the very low volume/surface area ratio of a single EPD (7.5 microliters/cm2), steady-state ADOi may remain constant during sampling, allowing for accurate determinations of ADOi with this method.

Adenosine↗